ST elevation myocardial infarction coronary angiography: Difference between revisions
Brian Blank (talk | contribs) No edit summary |
No edit summary |
||
| Line 1: | Line 1: | ||
{{Infobox_Disease | | {{Infobox_Disease | | ||
Name = Myocardial infarction| | Name = Myocardial infarction| | ||
| Line 27: | Line 26: | ||
{{main|Coronary catheterization}} | {{main|Coronary catheterization}} | ||
During coronary [[angiography]] a [[catheter]] is inserted into an artery (usually the [[femoral artery]]) and advanced over a wire to the vessels supplying the heart. Through the injection of dye, obstructed or narrowed coronary arteries can be identified, and [[angioplasty]] can be performed to open these occlusions. Angioplasty requires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by [[interventional cardiology|interventional cardiologists]]. | |||
== Pathophysiology of Reperfusion== | == Pathophysiology of Reperfusion== | ||
Revision as of 18:22, 11 February 2009
| Myocardial infarction | |
 | |
|---|---|
| Diagram of a myocardial infarction (2) of the tip of the anterior wall of the heart (an apical infarct) after occlusion (1) of a branch of the left coronary artery (LCA, right coronary artery = RCA). | |
| ICD-10 | I21-I22 |
| ICD-9 | 410 |
| DiseasesDB | 8664 |
| MedlinePlus | 000195 |
| eMedicine | med/1567 emerg/327 ped/2520 |
| Cardiology Network |
 Discuss ST elevation myocardial infarction coronary angiography further in the WikiDoc Cardiology Network |
| Adult Congenital |
|---|
| Biomarkers |
| Cardiac Rehabilitation |
| Congestive Heart Failure |
| CT Angiography |
| Echocardiography |
| Electrophysiology |
| Cardiology General |
| Genetics |
| Health Economics |
| Hypertension |
| Interventional Cardiology |
| MRI |
| Nuclear Cardiology |
| Peripheral Arterial Disease |
| Prevention |
| Public Policy |
| Pulmonary Embolism |
| Stable Angina |
| Valvular Heart Disease |
| Vascular Medicine |
Editor-In-Chief: C. Michael Gibson, M.S., M.D. [1]
Associate Editor-In-Chief: Cafer Zorkun, M.D., Ph.D. [2]
Please Join in Editing This Page and Apply to be an Editor-In-Chief for this topic: There can be one or more than one Editor-In-Chief. You may also apply to be an Associate Editor-In-Chief of one of the subtopics below. Please mail us [3] to indicate your interest in serving either as an Editor-In-Chief of the entire topic or as an Associate Editor-In-Chief for a subtopic. Please be sure to attach your CV and or biographical sketch.
Angiography
During coronary angiography a catheter is inserted into an artery (usually the femoral artery) and advanced over a wire to the vessels supplying the heart. Through the injection of dye, obstructed or narrowed coronary arteries can be identified, and angioplasty can be performed to open these occlusions. Angioplasty requires extensive skill, especially in emergency settings, and may not always be available out of hours. It is commonly performed by interventional cardiologists.
Pathophysiology of Reperfusion
The Importance of Restoring and Sustaining Complete Epicardial and Myocardial Perfusion
Recently, it has become recognized that it is necessary but not sufficient to restore epicardial flow in ST elevation MI. Not all TIMI grade 3 flow is created equally. In addition to epicardial flow, myocardial perfusion must be restored as well. This has been demonstrated in both myocardial contrast echo studies as well as angiographic studies[1][2][3][4][5][6][7][8][9][10][11][12][13]. As a result of this new understanding, the goal of reperfusion therapies has shifted to include reperfusion downstream at the level of capillary bed, and it might be more appropriate that the current reperfusion hypothesis now be termed "the time dependent open muscle hypothesis." This wiki article reviews the angiographic methods used to evaluate myocardial ischemia and infarction and discusses the insights into the pathophysiology of acute coronary syndromes provided by these angiographic indexes of coronary artery blood flow and myocardial perfusion.
TIMI Flow Grades (TFGs)
The Thrombolysis In Myocardial Infarction (TIMI) flow grade classification scheme has been widely used to assess coronary blood flow in acute coronary syndromes [1]. TFG 0 means the artery is closed; TFG 1 means that dye penetrates the stenosis but does not reach the downstream bed; TFG 2 means that flow is slow down the artery and TFG 3 means that normal flow has been restored. The association of the TFGs with clinical outcomes (including mortality) has been well documented [2][3][4][5][6][7][8].
The association of the TFGs with mortality must be interpreted with caution as there are several confounders:
- The majority of TIMI grade 2 flow is observed in the left anterior descending artery (LAD) territory, whereas the majority of TIMI grade 3 flow is observed in the right coronary artery (RCA)[7]. Thus, the improved mortality observed among patients with TIMI grade 3 flow may be explained at least in part by the fact that inferior myocardial infarction (MI) location is associated with a lower mortality rate [7].
- The clinical improvement associated with TIMI grade 3 flow may have be nonlinear. For example, greater clinical benefits may be observed if a closed artery (TFG 0/1) is opened (TFG 2) compared with the improvement that might occur if an artery with TFG 2 is converted to TFG 3 flow.
- As more arteries with TFG 2 flow are treated with adjunctive percutaneous coronary intervention (PCI), the prognosis associated with this flow grade may improve. The fact that patients who were treated with an inferior fibrinolytic monotherapy strategy faired so well in GUSTO V may be explained in part by the fact that these patients underwent PCI more often[14]. Two-year follow-up in more recent studies indicates that the survival advantage of TFG 3 flow over TFG 2 flow at 2 years may not be as great as it once was in the era before aggressive utilization of rescue and adjunctive (PCI)[10].
Reocclusion
While PCI may obviously improve epicardial flow, another often unrecognized benefit is the fact that rescue PCI (dilating a closed artery) and adjunctive PCI (dilating an open artery) following fibrinolytic administration may reduce the risk of reocclusion. Reinfarction doubles early mortality by 30 days[14][15]. Controversy has surrounded the use of PCI immediately following PCI, and for many years, immediate PCI was classified as a class III contraindication. These early trials preceded the use of stents, thienopyridines, platelet GP IIb/IIIa inhibitors, and the monitoring of activated clotting times. Among 20 101 patients enrolled in recent TIMI trials, Gibson et al have reported that the performance of PCI during the index hospitalization was associated with a lower rate of in-hospital recurrent MI (1.6% versus 4.5%, P<0.001) and a lower 2-year mortality (5.6% versus 11.6%, P<0.001)[15][16]. In addition to flow other nonangiographic findings and processes may also underlie the pathophysiology of reocclusion as well as other clinical outcomes [17].
The TIMI Frame Count: A More Precise Angiographic Index of Coronary Blood Flow
There are several limitations to the TFG classification scheme[7]. To overcome these limitations, Gibson developed a more objective and precise index of coronary blood flow called the corrected TIMI frame count (CTFC). In this method, the number of cineframes required for dye to reach standardized distal landmarks are counted. Each frame is 1/30th of a second, and the angiogram is therefore essentially a measure of the time for dye to go down the artery[7][8][10]. In the first frame used for TIMI frame counting, a column of dye touches both borders of the coronary artery and moves forward[7]. In the last frame, dye begins to enter (but does not necessarily fill) a standard distal landmark in the artery. These standard distal landmarks are as follows: in the RCA, the first branch of the posterolateral artery; in the circumflex system, the most distal branch of the obtuse marginal branch, which includes the culprit lesion in the dye path; and in the LAD, the distal bifurcation, which is also known as the "moustache," "pitchfork" or "whale’s tail". These frame counts are corrected for the longer length of the LAD by dividing by 1.7 to arrive at the CTFC [7]. Knowing the time for dye to go down the artery from the CTFC (CTFC/30=seconds), and length of the artery (either from an angioplasty guide wire or by planimetry), dye velocity (cm/s) can also be calculated in a more refined fashion.19 This refined measure allows calculation of the velocity proximal and distal to the lesion[18].
Some of the advantages of the TIMI frame count method are as follows. In contrast to the TFG classification scheme, the CTFC is quantitative rather than qualitative, it is objective rather than subjective, it is a continuous rather than a categorical variable, and it is reproducible[7]. The CTFC demonstrates that flow is not divided into arbitrary slow and fast categories, but rather coronary blood flow is unimodally distributed as a continuous variable[7]. The CTFC has been shown to be quite reproducible with a 1- to 2-frame difference between observers [19][20][21][22][23][24][25][26][27][28][25][26][29]. The CTFC is also highly correlated with other measures of flow such as Doppler velocity wire measures of coronary flow reserve, distal velocity, average peak velocity, and volumetric flow, [20][21][22] as well as fractional flow reserve (r=0.85)[23].
Several technical and physiological variables may impact the CTFC[19][30][31][32][33]:
- Injection force: A power injector to change the force of injection (cc/sec) from the 10th to the 90th percentile of human injection rates lowers the CTFC by only 2 frames[30].
- Nitrate administration significantly increases the CTFC by 6 frames (P<0.001)[19].
- Dye injection at the beginning of diastole decreases the CTFC by 3 to 6 frames[19].
- Increasing the heart rate by 20 beats per minute significantly decreases the CTFC by 5 frames (P<0.001)[19].
Association of the CTFC with Clinical Outcomes
Following fibrinolytic administration as well as PCI, the CTFC is related to a variety of clinical outcomes [7][8][10][24][25][26][27]. Flow in the infarct-related artery in survivors is significantly faster than in patients who die (49.5 versus 69.6 frames; P=0.0003)[8]. In NSTEMI and STEMI, the post-PCI culprit flow among survivors is significantly faster than among those patients who died (CTFCs 20.4 versus 33.4 frames, P=0.017)(37). Among patients undergoing PCI, the CTFC has demonstrated greater sensitivity in detecting improvements in epicardial flow compared with the use of TIMI grade 3 flow among patients treated with new device interventions and in the detection of transplant rejection [34][35][36][37][38][39].
The Pathophysiology of STEMI and UA/NSTEMI Based on measures of epicardial flow
One of the more interesting observations learned with the use of the CTFC is the fact that flow in nonculprit arteries in the setting of acute coronary syndromes is "abnormal." For instance, the CTFC in uninvolved arteries in acute STEMI (30.5 frames) is in fact 40% slower than normal (21 frames, P<0.001)[7][40][41][42]. Adjunctive and rescue PCI following fibrinolysis restores flow in culprit vessels that is nearly identical to that of nonculprit arteries in the STEMI setting (30.5 versus 30.5 frames, p=NS)[40], but this flow remains slower than normal (21 frames). It is notable that PCI of the culprit lesion is also associated with improvements in the nonculprit artery after the intervention in both the STEMI and UA/NSTEMI settings [40][41]. Slower flow throughout all 3 arteries in STEMI is associated with a higher risk of adverse outcomes[40], poorer wall motion in remote territories[40], poorer tissue perfusion on digital subtraction angiography (DSA)[41], and a greater magnitude of ST depression in remote territories such as the anterior precordium in inferior MI[43]. The basis of slowed flow in non-culprit arteries is not clear. It has been speculated that the delayed flow in the non-culprit artery may be the result of spasm in shared territories of microvasculature, or a result of global vasoconstriction mediated through either a local neurohumoral or paracrine mechanism. Gregorini et al[44] have highlighted the importance of sympathetic storm. Consistent with this hypothesis, they have demonstrated that the CTFC and fractional wall shortening is improved in both the culprit and nonculprit arteries after administration of alpha-blockers. Willerson and others [45][46][47][48][49][50][51] have also demonstrated that a wide range of vasoconstrictors including thromboxane A2, serotonin, endothelin, oxygen-derived free radicals, and thrombin are all released in the setting of vessel injury, thrombosis and reperfusion. While a residual stenosis following PCI in the setting of STEMI may be responsible for the delay in flow, it is important to note that despite a minimal 13% residual stenosis and the relief of intraluminal obstruction with stent placement, flow remains persistently abnormal in 34% of stented vessels[52].
Assessment of Myocardial Perfusion on the Angiogram: The TIMI Myocardial Perfusion Grade (TMPG)
Studies of myocardial constrast echocardiography (MCE) and angiography have demonstrated that restoration of epicardial flow does not necessarily lead to restoration of tissue level or microvascular perfusion [12][13]. Perfusion of the myocardium can also be assessed using the angiogram. In the TMPG system, TMPG 0 represents minimal or no myocardial blush; in TMPG 1, dye stains the myocardium, and this stain persists on the next injection; in TMPG 2, dye enters the myocardium but washes out slowly so that dye is strongly persistent at the end of the injection; and in TMPG 3, there is normal entrance and exit of dye in the myocardium (Table). Another method of assessing myocardial perfusion on the angiogram is the myocardial blush grade (MBG) developed by van’t Hof et al.57 A grade of 0 (no blush) and a grade of 3 (normal blush) are the same in the TMPG and MBG systems. An MBG grade 1 or 2 represents diminished intensity in the myocardium and corresponds to a value of 0.5 in the expanded TMPG grading system. A TMPG of 1 or a stain in the TIMI system is subsumed within the value of a 0 in the MBG system. Thus, normal perfusion in the myocardium carries a score of 3 in both the TMPG and MBG systems, and a closed muscle carries a score of 0 in both systems. Lepper et al58 have demonstrated that angiographic and echocardiographic myocardial perfusion are closely related, and among patients undergoing primary PCI for acute MI, impaired MBG was the best multivariate predictor of nonreperfusion on myocardial contrast echocardiography.
Independent of flow in the epicardial artery and other covariates such as age, blood pressure, and pulse, the TMPG has been shown to be multivariate predictors of mortality in acute STEMI at 2 years.10 The TMPG permits risk stratification even within epicardial TIMI grade 3 flow. Despite achieving epicardial patency with normal TIMI grade 3 flow, those patients whose microvasculature fails to open (TMPG 0/1) have a 7-fold increase in mortality compared with those patients with both TIMI grade 3 flow in the epicardial artery. Achievement of both TIMI grade 3 flow in both the artery and the myocardium is associated with a mortality under 1%10 (Figure 4). Likewise, in the setting of primary PCI, both van’t Hof et al57 and Haager et al59 have demonstrated an association between impaired myocardial perfusion and early and late mortality. These improvements in early and late mortality may be mediated by improvements in myocardial salvage.60 As Dibra et al60 have demonstrated, restoration of TMPG 2/3 is associated with a higher salvage index (0.49±0.42 versus 0.34±0.49, P=0.01) and a smaller final infarct size (15.4±15.5% versus 22.1±16.2% of the left ventricle, P=0.001). Indeed, second only to stent placement, restoration of TMPG 2/3 was the next most powerful independent determinant of the myocardial salvage index, and was more closely associated with higher salvage indexes than the TFGs.60
References
- ↑ 1.0 1.1 "The Thrombolysis in Myocardial Infarction (TIMI) trial. Phase I findings. TIMI Study Group". N. Engl. J. Med. 312 (14): 932–6. 1985. PMID 4038784. Unknown parameter
|month=ignored (help) - ↑ 2.0 2.1 Simes RJ, Topol EJ, Holmes DR; et al. (1995). "Link between the angiographic substudy and mortality outcomes in a large randomized trial of myocardial reperfusion. Importance of early and complete infarct artery reperfusion. GUSTO-I Investigators". Circulation. 91 (7): 1923–8. PMID 7895348. Unknown parameter
|month=ignored (help) - ↑ 3.0 3.1 "The effects of tissue plasminogen activator, streptokinase, or both on coronary-artery patency, ventricular function, and survival after acute myocardial infarction. The GUSTO Angiographic Investigators". N. Engl. J. Med. 329 (22): 1615–22. 1993. PMID 8232430. Unknown parameter
|month=ignored (help) - ↑ 4.0 4.1 Vogt A, von Essen R, Tebbe U, Feuerer W, Appel KF, Neuhaus KL (1993). "Impact of early perfusion status of the infarct-related artery on short-term mortality after thrombolysis for acute myocardial infarction: retrospective analysis of four German multicenter studies". J. Am. Coll. Cardiol. 21 (6): 1391–5. PMID 8473646. Unknown parameter
|month=ignored (help) - ↑ 5.0 5.1 Karagounis L, Sorensen SG, Menlove RL, Moreno F, Anderson JL (1992). "Does thrombolysis in myocardial infarction (TIMI) perfusion grade 2 represent a mostly patent artery or a mostly occluded artery? Enzymatic and electrocardiographic evidence from the TEAM-2 study. Second Multicenter Thrombolysis Trial of Eminase in Acute Myocardial Infarction". J. Am. Coll. Cardiol. 19 (1): 1–10. PMID 1729317. Unknown parameter
|month=ignored (help) - ↑ 6.0 6.1 Anderson JL, Karagounis LA, Becker LC, Sorensen SG, Menlove RL (1993). "TIMI perfusion grade 3 but not grade 2 results in improved outcome after thrombolysis for myocardial infarction. Ventriculographic, enzymatic, and electrocardiographic evidence from the TEAM-3 Study". Circulation. 87 (6): 1829–39. PMID 8504495. Unknown parameter
|month=ignored (help) - ↑ 7.00 7.01 7.02 7.03 7.04 7.05 7.06 7.07 7.08 7.09 7.10 7.11 Gibson CM, Cannon CP, Daley WL; et al. (1996). "TIMI frame count: a quantitative method of assessing coronary artery flow". Circulation. 93 (5): 879–88. PMID 8598078. Unknown parameter
|month=ignored (help) - ↑ 8.0 8.1 8.2 8.3 8.4 Gibson CM, Murphy SA, Rizzo MJ; et al. (1999). "Relationship between TIMI frame count and clinical outcomes after thrombolytic administration. Thrombolysis In Myocardial Infarction (TIMI) Study Group". Circulation. 99 (15): 1945–50. PMID 10208996. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Cannon CP, Murphy SA; et al. (2000). "Relationship of TIMI myocardial perfusion grade to mortality after administration of thrombolytic drugs". Circulation. 101 (2): 125–30. PMID 10637197. Unknown parameter
|month=ignored (help) - ↑ 10.0 10.1 10.2 10.3 Gibson CM, Cannon CP, Murphy SA, Marble SJ, Barron HV, Braunwald E (2002). "Relationship of the TIMI myocardial perfusion grades, flow grades, frame count, and percutaneous coronary intervention to long-term outcomes after thrombolytic administration in acute myocardial infarction". Circulation. 105 (16): 1909–13. PMID 11997276. Unknown parameter
|month=ignored (help) - ↑ Angeja BG, Gunda M, Murphy SA; et al. (2002). "TIMI myocardial perfusion grade and ST segment resolution: association with infarct size as assessed by single photon emission computed tomography imaging". Circulation. 105 (3): 282–5. PMID 11804979. Unknown parameter
|month=ignored (help) - ↑ 12.0 12.1 Ito H, Tomooka T, Sakai N; et al. (1992). "Lack of myocardial perfusion immediately after successful thrombolysis. A predictor of poor recovery of left ventricular function in anterior myocardial infarction". Circulation. 85 (5): 1699–705. PMID 1572028. Unknown parameter
|month=ignored (help) - ↑ 13.0 13.1 Ito H, Maruyama A, Iwakura K; et al. (1996). "Clinical implications of the 'no reflow' phenomenon. A predictor of complications and left ventricular remodeling in reperfused anterior wall myocardial infarction". Circulation. 93 (2): 223–8. PMID 8548892. Unknown parameter
|month=ignored (help) - ↑ 14.0 14.1 Hudson MP, Granger CB, Topol EJ; et al. (2001). "Early reinfarction after fibrinolysis: experience from the global utilization of streptokinase and tissue plasminogen activator (alteplase) for occluded coronary arteries (GUSTO I) and global use of strategies to open occluded coronary arteries (GUSTO III) trials". Circulation. 104 (11): 1229–35. PMID 11551872. Unknown parameter
|month=ignored (help) - ↑ 15.0 15.1 Gibson CM, Karha J, Murphy SA; et al. (2003). "Early and long-term clinical outcomes associated with reinfarction following fibrinolytic administration in the Thrombolysis in Myocardial Infarction trials". J. Am. Coll. Cardiol. 42 (1): 7–16. PMID 12849652. Unknown parameter
|month=ignored (help) - ↑ Gibson CM (2000). "A union in reperfusion: the concept of facilitated percutaneous coronary intervention". J. Am. Coll. Cardiol. 36 (5): 1497–9. PMID 11079648. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Cannon CP, Piana RN; et al. (1995). "Angiographic predictors of reocclusion after thrombolysis: results from the Thrombolysis in Myocardial Infarction (TIMI) 4 trial". J. Am. Coll. Cardiol. 25 (3): 582–9. PMID 7860900. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Dodge JT, Goel M; et al. (1997). "Angioplasty guidewire velocity: a new simple method to calculate absolute coronary blood velocity and flow". Am. J. Cardiol. 80 (12): 1536–9. PMID 9416931. Unknown parameter
|month=ignored (help) - ↑ 19.0 19.1 19.2 19.3 19.4 Abaci A, Oguzhan A, Eryol NK, Ergin A (1999). "Effect of potential confounding factors on the thrombolysis in myocardial infarction (TIMI) trial frame count and its reproducibility". Circulation. 100 (22): 2219–23. PMID 10577994. Unknown parameter
|month=ignored (help) - ↑ 20.0 20.1 Manginas A, Gatzov P, Chasikidis C, Voudris V, Pavlides G, Cokkinos DV (1999). "Estimation of coronary flow reserve using the Thrombolysis In Myocardial Infarction (TIMI) frame count method". Am. J. Cardiol. 83 (11): 1562–5, A7. PMID 10363873. Unknown parameter
|month=ignored (help) - ↑ 21.0 21.1 Stankovic G, Manginas A, Voudris V; et al. (2000). "Prediction of restenosis after coronary angioplasty by use of a new index: TIMI frame count/minimal luminal diameter ratio". Circulation. 101 (9): 962–8. PMID 10704161. Unknown parameter
|month=ignored (help) - ↑ 22.0 22.1 Barcin C, Denktas AE, Garratt KN, Higano ST, Holmes DR, Lerman A (2003). "Relation of Thrombolysis in Myocardial Infarction (TIMI) frame count to coronary flow parameters". Am. J. Cardiol. 91 (4): 466–9. PMID 12586269. Unknown parameter
|month=ignored (help) - ↑ 23.0 23.1 Umman B, Nisanci Y, Sezer M; et al. (2002). "The relationship between corrected TIMI frame count and myocardial fractional flow reserve". J Invasive Cardiol. 14 (3): 125–8. PMID 11870267. Unknown parameter
|month=ignored (help) - ↑ 24.0 24.1 French JK, Ellis CJ, Webber BJ; et al. (1998). "Abnormal coronary flow in infarct arteries 1 year after myocardial infarction is predicted at 4 weeks by corrected Thrombolysis in Myocardial Infarction (TIMI) frame count and stenosis severity". Am. J. Cardiol. 81 (6): 665–71. PMID 9527071. Unknown parameter
|month=ignored (help) - ↑ 25.0 25.1 25.2 French JK, Straznicky IT, Webber BJ; et al. (1999). "Angiographic frame counts 90 minutes after streptokinase predict left ventricular function at 48 hours following myocardial infarction". Heart. 81 (2): 128–33. PMC 1728934. PMID 9922346. Unknown parameter
|month=ignored (help) - ↑ 26.0 26.1 26.2 French JK, Hyde TA, Straznicky IT; et al. (2000). "Relationship between corrected TIMI frame counts at three weeks and late survival after myocardial infarction". J. Am. Coll. Cardiol. 35 (6): 1516–24. PMID 10807455. Unknown parameter
|month=ignored (help) - ↑ 27.0 27.1 Amos DJ, French JK, Andrews J; et al. (2001). "Corrected TIMI frame counts correlate with stenosis severity and infarct zone wall motion after thrombolytic therapy". Am. Heart J. 141 (4): 586–91. doi:10.1067/mhj.2001.113393. PMID 11275924. Unknown parameter
|month=ignored (help) - ↑ Sahin M, Basoglu T, Canbaz F, Elcik M, Kosus A (2002). "The value of the TIMI frame count method in the diagnosis of coronary no-reflow: a comparison with myocardial perfusion SPECT in patients with acute myocardial infarction". Nucl Med Commun. 23 (12): 1205–10. doi:10.1097/01.mnm.0000046213.83338.9e. PMID 12464786. Unknown parameter
|month=ignored (help) - ↑ Topol EJ, Ohman EM, Armstrong PW; et al. (2000). "Survival outcomes 1 year after reperfusion therapy with either alteplase or reteplase for acute myocardial infarction: results from the Global Utilization of Streptokinase and t-PA for Occluded Coronary Arteries (GUSTO) III Trial". Circulation. 102 (15): 1761–5. PMID 11023929. Unknown parameter
|month=ignored (help) - ↑ 30.0 30.1 Dodge JT, Rizzo M, Nykiel M; et al. (1998). "Impact of injection rate on the Thrombolysis in Myocardial Infarction (TIMI) trial frame count". Am. J. Cardiol. 81 (10): 1268–70. PMID 9604968. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Anshelevich M, Murphy S; et al. (2000). "Impact of injections during diagnostic coronary arteriography on coronary patency in the setting of acute myocardial infarction from the TIMI trials. Thrombolysis In Myocardial Infarction". Am. J. Cardiol. 86 (12): 1378–9, A5. PMID 11113418. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Kirtane AJ, Murphy SA; et al. (2001). "Impact of contrast agent type (ionic versus nonionic) used for coronary angiography on angiographic, electrocardiographic, and clinical outcomes following thrombolytic administration in acute myocardial infarction". Catheter Cardiovasc Interv. 53 (1): 6–11. doi:10.1002/ccd.1121. PMID 11329210. Unknown parameter
|month=ignored (help) - ↑ Faile BA, Guzzo JA, Tate DA, Nichols TC, Smith SC, Dehmer GJ (2000). "Effect of sex, hemodynamics, body size, and other clinical variables on the corrected thrombolysis in myocardial infarction frame count used as an assessment of coronary blood flow". Am. Heart J. 140 (2): 308–14. doi:10.1067/mhj.2000.108003. PMID 10925348. Unknown parameter
|month=ignored (help) - ↑ Edep ME, Guarneri EM, Teirstein PS, Phillips PS, Brown DL (1999). "Differences in TIMI frame count following successful reperfusion with stenting or percutaneous transluminal coronary angioplasty for acute myocardial infarction". Am. J. Cardiol. 83 (9): 1326–9. PMID 10235089. Unknown parameter
|month=ignored (help) - ↑ Vrachatis AD, Alpert MA, Georgulas VP; et al. (2001). "Comparative efficacy of primary angioplasty with stent implantation and thrombolysis in restoring basal coronary artery flow in acute ST segment elevation myocardial infarction: quantitative assessment using the corrected TIMI frame count". Angiology. 52 (3): 161–6. PMID 11269778. Unknown parameter
|month=ignored (help) - ↑ Hamada S, Nishiue T, Nakamura S; et al. (2001). "TIMI frame count immediately after primary coronary angioplasty as a predictor of functional recovery in patients with TIMI 3 reperfused acute myocardial infarction". J. Am. Coll. Cardiol. 38 (3): 666–71. PMID 11527614. Unknown parameter
|month=ignored (help) - ↑ Capozzolo C, Piscione F, De Luca G; et al. (2001). "Direct coronary stenting: effect on coronary blood flow, immediate and late clinical results". Catheter Cardiovasc Interv. 53 (4): 464–73. PMID 11514995. Unknown parameter
|month=ignored (help) - ↑ Bickel C, Rupprecht HJ, Maimaitiming A; et al. (2002). "The superiority of TIMI frame count in detecting coronary flow changes after coronary stenting compared to TIMI Flow Classification". J Invasive Cardiol. 14 (10): 590–6. PMID 12368511. Unknown parameter
|month=ignored (help) - ↑ Fang JC, Kinlay S, Wexberg P; et al. (2000). "Use of the thrombolysis in myocardial infarction frame count for the quantitative assessment of transplant-associated arteriosclerosis". Am. J. Cardiol. 86 (8): 890–2. PMID 11024410. Unknown parameter
|month=ignored (help) - ↑ 40.0 40.1 40.2 40.3 40.4 Gibson CM, Ryan KA, Murphy SA; et al. (1999). "Impaired coronary blood flow in nonculprit arteries in the setting of acute myocardial infarction. The TIMI Study Group. Thrombolysis in myocardial infarction". J. Am. Coll. Cardiol. 34 (4): 974–82. PMID 10520778. Unknown parameter
|month=ignored (help) - ↑ 41.0 41.1 41.2 Gibson CM, Goel M, Murphy SA; et al. (2000). "Global impairment of coronary blood flow in the setting of acute coronary syndromes (a RESTORE substudy). Randomized Efficacy Study of Tirofiban for Outcomes and Restenosis". Am. J. Cardiol. 86 (12): 1375–7, A5. PMID 11113417. Unknown parameter
|month=ignored (help) - ↑ Goldstein JA, Demetriou D, Grines CL, Pica M, Shoukfeh M, O'Neill WW (2000). "Multiple complex coronary plaques in patients with acute myocardial infarction". N. Engl. J. Med. 343 (13): 915–22. PMID 11006367. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Chen M, Angeja BG; et al. (2002). "Precordial ST-segment depression in inferior myocardial infarction is associated with slow flow in the non-culprit left anterior descending artery" (PDF). J. Thromb. Thrombolysis. 13 (1): 9–12. PMID 11994554. Unknown parameter
|month=ignored (help) - ↑ Gregorini L, Marco J, Kozàkovà M; et al. (1999). "Alpha-adrenergic blockade improves recovery of myocardial perfusion and function after coronary stenting in patients with acute myocardial infarction". Circulation. 99 (4): 482–90. PMID 9927393. Unknown parameter
|month=ignored (help) - ↑ Hirsh PD, Hillis LD, Campbell WB, Firth BG, Willerson JT (1981). "Release of prostaglandins and thromboxane into the coronary circulation in patients with ischemic heart disease". N. Engl. J. Med. 304 (12): 685–91. PMID 6894016. Unknown parameter
|month=ignored (help) - ↑ Bush LR, Campbell WB, Kern K; et al. (1984). "The effects of alpha 2-adrenergic and serotonergic receptor antagonists on cyclic blood flow alterations in stenosed canine coronary arteries". Circ. Res. 55 (5): 642–52. PMID 6488486. Unknown parameter
|month=ignored (help) - ↑ Willerson JT, Campbell WB, Winniford MD; et al. (1984). "Conversion from chronic to acute coronary artery disease: speculation regarding mechanisms". Am. J. Cardiol. 54 (10): 1349–54. PMID 6391133. Unknown parameter
|month=ignored (help) - ↑ Apprill P, Schmitz JM, Campbell WB; et al. (1985). "Cyclic blood flow variations induced by platelet-activating factor in stenosed canine coronary arteries despite inhibition of thromboxane synthetase, serotonin receptors, and alpha-adrenergic receptors". Circulation. 72 (2): 397–405. PMID 2988822. Unknown parameter
|month=ignored (help) - ↑ Ashton JH, Golino P, McNatt JM, Buja LM, Willerson JT (1989). "Serotonin S2 and thromboxane A2-prostaglandin H2 receptor blockade provide protection against epinephrine-induced cyclic flow variations in severely narrowed canine coronary arteries". J. Am. Coll. Cardiol. 13 (3): 755–63. PMID 2521875. Unknown parameter
|month=ignored (help) - ↑ Eidt JF, Allison P, Noble S; et al. (1989). "Thrombin is an important mediator of platelet aggregation in stenosed canine coronary arteries with endothelial injury". J. Clin. Invest. 84 (1): 18–27. doi:10.1172/JCI114138. PMC 303947. PMID 2661588. Unknown parameter
|month=ignored (help) - ↑ Willerson JT, Golino P, Eidt J, Campbell WB, Buja LM (1989). "Specific platelet mediators and unstable coronary artery lesions. Experimental evidence and potential clinical implications". Circulation. 80 (1): 198–205. PMID 2661053. Unknown parameter
|month=ignored (help) - ↑ Gibson CM, Murphy S, Menown IB; et al. (1999). "Determinants of coronary blood flow after thrombolytic administration. TIMI Study Group. Thrombolysis in Myocardial Infarction". J. Am. Coll. Cardiol. 34 (5): 1403–12. PMID 10551685. Unknown parameter
|month=ignored (help)
See also
- acute coronary syndrome
- angina
- Cardiac arrest
- coronary thrombosis
- Hibernating myocardium
- Stunned myocardium
- Ventricular remodeling
External links
- The MD TV: Comments on Hot Topics, State of the Art Presentations in Cardiovascular Medicine, Expert Reviews on Cardiovascular Research
- Clinical Trial Results: An up to dated resource of Cardiovascular Research
- Risk Assessment Tool for Estimating Your 10-year Risk of Having a Heart Attack - based on information of the Framingham Heart Study, from the United States National Heart, Lung and Blood Institute
- Heart Attack - overview of resources from MedlinePlus.
- Heart Attack Warning Signals from the Heart and Stroke Foundation of Canada
- Regional PCI for STEMI Resource Center - Evidence based online resource center for the development of regional PCI networks for acute STEMI
- STEMI Systems - Articles, profiles, and reviews of the latest publications involved in STEMI care. Quarterly newsletter.
- American College of Cardiology (ACC) Door to Balloon (D2B) Initiative.
- American Heart Association's Heart Attack web site - Information and resources for preventing, recognizing and treating heart attack.